In studies of obsessive-compulsive disorder (OCD) co-morbidity, OCD patients assessed by structured diagnostic interviews were found to have an increased incidence of lifetime diagnosis of anorexia nervosa and bulimia nervosa. In a separate study, patients with idiopathic spasmodic torticollis were found to have significantly more OCD-related symptoms than healthy controls. In psychobiologic, patients with OCD were found to have elevated CSF levels of somatostatin. The degree of somatostatin elevation was related to the degree of elevation of two other stress-responsive, arousal- producing neuropeptides: corticotropin releasing hormone and vasopressin. A methodological study of variables affecting the tendency of m-CCP, a 5-HT1C receptor agonist, to exacerbate OCD symptoms, helped to reconcile discrepancies in the literature on the behavioral effects of this serotonergic agent. Patients with OCD and a related disorder, trichotillomania, had no abnormalities on an extensive battery of neuropsychological tests designed to assess basal ganglia processing, a finding in at least partial conflict with the current conception of OCD as a product of basal ganglia dysfunction. In treatment efficacy studies, compared to placebo, trazodone, a preferential serotonin (5-HT) antagonist and weak reuptake inhibitor, did not reduce OCD symptoms. Augmentation with buspirone, a 5-HT1A agonist did not further enhance symptom reduction in a group of patients who had been receiving long-term fluoxetine treatment. In preclinical studies, serotonin reuptake blockers given chronically were distinguished from antidepressants not effective for OCD treatment by an ability to decrease hypothalamic secretion of vasopressin, a peptide which we had previously found to be hypersecreted into the CSF and plasma of patients with OCD.